甲状腺功能亢进性心脏的无氧运动能力与代谢

Anaerobic performance and metabolism of the hyperthyroid heart.

作者信息

Altschuld R A, Weiss A, Kruger F A, Weissler A M

出版信息

J Clin Invest. 1969 Oct;48(10):1905-13. doi: 10.1172/JCI106157.

DOI:10.1172/JCI106157

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC322427/

Abstract

Anaerobically periused hearts from rats with experimentally induced hyperthyroidism exhibited accelerated deterioration of pacemaker activity and ventricular performance. The diminished anaerobic performance of hyperthyroid hearts was associated with decreased adenosine triphosphate (ATP) levels and a reduced rate of anaerobic glycolysis as reflected in decreased lactic acid production during 30 min of anoxic perfusion.Studies on whole heart homogenates demonstrated inhibition at the phosphofructokinase (PFK) step of the glycolytic pathway. Such inhibition was not demonstrated in the hyperthyroid heart cytosol. It is postulated that an inhibitor of PFK which resides dominantly in the particulate fraction is probably responsible for the diminished anaerobic glycolysis and performance of the hyperthyroid heart.

摘要

对实验性诱导甲状腺功能亢进大鼠的心脏进行无氧灌注时，发现其起搏器活动和心室功能加速恶化。甲状腺功能亢进心脏的无氧功能下降与三磷酸腺苷（ATP）水平降低以及无氧糖酵解速率降低有关，这在30分钟缺氧灌注期间乳酸生成减少中得到体现。对全心脏匀浆的研究表明，糖酵解途径的磷酸果糖激酶（PFK）步骤受到抑制。而在甲状腺功能亢进心脏的细胞溶胶中未发现这种抑制作用。据推测，主要存在于颗粒部分的PFK抑制剂可能是导致甲状腺功能亢进心脏无氧糖酵解和功能下降的原因。

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本文引用的文献

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